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Long-term Potentiation

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term Potentiation01:25

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Calmodulin-dependent Signaling01:16

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Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
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Related Experiment Video

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Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents
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CaMKII: a molecular substrate for synaptic plasticity and memory.

Brian C Shonesy1, Nidhi Jalan-Sakrikar1, Victoria S Cavener2

  • 1Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.

Progress in Molecular Biology and Translational Science
|February 4, 2014
PubMed
Summary
This summary is machine-generated.

Calcium-calmodulin-dependent protein kinase II (CaMKII) acts as a molecular switch, becoming constitutively active after calcium influx during long-term potentiation (LTP). This sustained CaMKII activation is crucial for synaptic plasticity, learning, and memory.

Keywords:
AMPA receptorsCaMKIICalcium/calmodulin-dependent protein kinase IIHippocampusLTDLTPLong-term depressionLong-term potentiationMemoryNMDA receptorsSynaptic plasticity

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Biology

Background:

  • Learning and memory are attributed to alterations in neuronal circuit connectivity via synaptic plasticity.
  • Calcium influx during long-term potentiation (LTP) induction activates CaMKII in dendritic spines.

Purpose of the Study:

  • To discuss the molecular switch mechanism of CaMKII activation.
  • To explore the downstream targets of CaMKII in synaptic plasticity.

Main Methods:

  • Review of existing literature on CaMKII function in synaptic plasticity.
  • Discussion of CaMKII autophosphorylation as a molecular switch.
  • Analysis of CaMKII's role in modulating synaptic structure and function.

Main Results:

  • CaMKII activation via autophosphorylation creates a sustained "molecular switch".
  • This sustained activity is critical for LTP, learning, and memory.
  • CaMKII regulates diverse downstream targets influencing synaptic dynamics.

Conclusions:

  • The CaMKII "molecular switch" is essential for synaptic plasticity and cognitive functions.
  • Understanding CaMKII's downstream targets provides insights into dynamic control of synaptic function.